Why the study?
Does treatment with benazepril, valsartan, or their combination reduce serum TGF-beta1 and microalbuminuria in patients with essential hypertension?
Does treatment with benazepril, valsartan, or their combination reduce serum TGF-beta1 and microalbuminuria in patients with essential hypertension?
Treatment with ACE inhibitors, ARBs, or their combination reduces serum TGF-beta1 and microalbuminuria in essential hypertension, suggesting a renoprotective effect.
May support renoprotective effects of ACEI/ARB therapy in hypertension; leaves open need for RCTs on hard renal outcomes.
BACKGROUND: Evidence suggests that transforming growth factor-beta1 (TGF-beta(1)) is associated with target organ damage in hypertension. This study aimed to investigate the relationship between TGF-beta(1) levels and kidney damage and renoprotective effects of angiotensin-converting enzyme inhibitor and/or angiotensin II type 1 receptor blocker in patients with essential hypertension (EH). METHODS: A total of 156 patients with EH were enrolled and grouped according to albumin-to-creatinine ratio (ACR). Of these, 90 patients with EH underwent a 12-week antihypertensive trial with administration of benazepril, valsartan or both. Serum TGF-beta(1), plasma angiotensin (Ang) II and urinary albumin were quantified by immunoassays. RESULTS: Serum TGF-beta1, plasma Ang II and ACR were highly elevated in patients with EH (P < 0.01). There was a positive correlation between serum TGF-beta1 levels and ACR (r = 0.53, P < 0.01). Significant decreases in TGF beta1 and ACR were obtained in all groups at the end of 12-week antihypertensive therapy compared to the baseline values, with the combined group to a greater extent (P < 0.01). Plasma Ang II levels were significantly decreased in the benazepril group but increased in the valsartan group (P < 0.05) while no significant change was observed in the combined group. CONCLUSIONS: TGF-beta(1) is highly elevated and strongly associated with urinary albumin excretion in patients with EH. Treatment with benazepril or valsartan attenuates serum TGF-beta(1) levels and microalbuminuria with the combined therapy receiving the greater effect. TGF-beta(1) could be a potential surrogate marker in monitoring the development and progression of kidney damage in EH.
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Zhu et al. (2008) studied this question.
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